FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3005264705> ?p ?o ?g. }

• W3005264705 endingPage "732" @default.
• W3005264705 startingPage "725" @default.
• W3005264705 abstract "Free AccessScientific InvestigationsComparison of upper airway obstruction during zolpidem-induced sleep and propofol-induced sleep in patients with obstructive sleep apnea: a pilot study Alexandre Beraldo Ordones, MD, Gustavo Freitas Grad, MD, Michel Burihan Cahali, MD, Geraldo Lorenzi-Filho, MD, Luiz Ubirajara Sennes, MD, Pedro Rodrigues Genta, MD Alexandre Beraldo Ordones, MD Department of Otolaryngology, Universidade de São Paulo, São Paulo, Brazil Search for more papers by this author , Gustavo Freitas Grad, MD Pulmonary Division, Heart Institute (InCor), Universidade de São Paulo, São Paulo, Brazil Search for more papers by this author , Michel Burihan Cahali, MD Department of Otolaryngology, Universidade de São Paulo, São Paulo, Brazil Search for more papers by this author , Geraldo Lorenzi-Filho, MD Pulmonary Division, Heart Institute (InCor), Universidade de São Paulo, São Paulo, Brazil Search for more papers by this author , Luiz Ubirajara Sennes, MD Department of Otolaryngology, Universidade de São Paulo, São Paulo, Brazil Search for more papers by this author , Pedro Rodrigues Genta, MD Pulmonary Division, Heart Institute (InCor), Universidade de São Paulo, São Paulo, Brazil Search for more papers by this author Published Online:May 15, 2020https://doi.org/10.5664/jcsm.8334Cited by:4SectionsAbstractPDF ShareShare onFacebookTwitterLinkedInRedditEmail ToolsAdd to favoritesDownload CitationsTrack Citations AboutABSTRACTStudy Objectives:Drug-induced sleep endoscopy (DISE) using propofol is commonly used to identify the pharyngeal structure involved in collapse among patients with obstructive sleep apnea. DISE has never been compared with zolpidem-induced sleep endoscopy. We hypothesized that propofol at recommended sedation levels does not influence upper airway collapsibility nor the frequency of multilevel pharyngeal collapse as compared with zolpidem-induced sleep.Methods:Twenty-one patients with obstructive sleep apnea underwent polysomnography and sleep endoscopy during zolpidem-induced sleep and during DISE with propofol. A propofol target-controlled infusion was titrated to achieve a bispectral index between 50 and 70. Airway collapsibility was estimated and compared in both conditions by peak inspiratory flow and the magnitude of negative effort dependence. Respiratory drive was estimated by the difference between end-expiratory and peak-negative inspiratory pharyngeal pressure (driving pressure). Site and configuration of pharyngeal collapse during zolpidem-induced sleep and DISE with propofol were compared.Results:The frequency of multilevel collapse during zolpidem-induced sleep was similar to that observed during DISE with propofol (72% vs 86%, respectively; difference: 14%; 95% confidence interval: −12% to 40%; P = .453). The endoscopic classification of pharyngeal collapse during both conditions were similar. Peak inspiratory flow, respiratory drive (effect size: 0.05 and 0.03, respectively), and negative effort dependence (difference: −6%; 95% confidence interval: −16% to 4%) were also similar in both procedures.Conclusions:In this pilot study, recommended propofol doses did not significantly increase multilevel pharyngeal collapse or affect upper airway collapsibility and respiratory drive as compared with zolpidem-induced sleep.Clinical Trial Registration:Registry: clinicaltrials.gov; Name: Natural and Drug Sleep Endoscopy; URL: https://clinicaltrials.gov/ct2/show/study/NCT03004014; Identifier: NCT03004014.Citation:Ordones AB, Grad GF, Cahali MB, Lorenzi-Filho G, Sennes LU, Genta PR. Comparison of upper airway obstruction during zolpidem-induced sleep and propofol-induced sleep in patients with obstructive sleep apnea: a pilot study. J Clin Sleep Med. 2020;16(5):725–732.BRIEF SUMMARYCurrent Knowledge/Study Rationale: Drug-induced sleep endoscopy with propofol is used to identify the site of collapse of the airway in patients with obstructive sleep apnea. However, propofol may increase upper airway collapsibility.Study Impact: Drug-induced sleep endoscopy with propofol has never been compared with zolpidem-induced sleep endoscopy; therefore, we performed endoscopy during zolpidem-induced sleep and drug-induced sleep endoscopy with propofol in patients with obstructive sleep apnea. Propofol used at the recommended sedation levels does not influence the results of sleep endoscopy as compared with zolpidem-induced sleep.INTRODUCTIONObstructive sleep apnea (OSA) is a common disorder characterized by repetitive pharyngeal collapse during sleep.1,2 One or more pharyngeal structures may collapse during sleep in patients with OSA, including the soft palate, lateral pharyngeal walls, tongue base, and epiglottis. The recognition of the pharyngeal structure involved in collapse allows site-specific treatment for OSA.3,4Drug-induced sleep endoscopy (DISE) has been used since 1991 to identify the pharyngeal structures causing collapse.5–9 The major applications of DISE are to guide the surgical approach for OSA, including the selection of candidates for hypoglossal nerve stimulation.8,10–12 Although sleep induction using sedatives has been used to facilitate the endoscopic procedure, DISE has never been compared with zolpidem-induced sleep endoscopy.13 We have previously shown that low levels of midazolam did not increase upper airway collapsibility.14 Currently, DISE is most commonly performed under propofol sedation, frequently without sedation depth monitoring.15 Upper airway collapsibility, respiratory drive, and site and configuration of pharyngeal collapse change according to depth of sedation during incremental propofol dose.16–20 Reports of DISE under propofol sedation have shown that up to 76% of individuals with OSA have >1 pharyngeal structure involved in airway obstruction.7,9,21,22 The influence of propofol sedation in multisite pharyngeal collapse is not known.The amplitude of inspiratory flow as measured by peak inspiratory flow during inspiratory flow limitation has been shown to be associated with airway collapsibility and airway dimensions.23 Negative effort dependence (NED), defined as the percentage reduction from peak to midinspiratory flow, reflects the interaction between respiratory effort and the dynamic compliance of the structure responsible for collapse.24 Sedatives could possibly influence NED by either decreasing respiratory effort or increasing the compliance of the pharyngeal structure involved in collapse.24We hypothesized that propofol at recommended sedation levels (bispectral index [BIS]: 50 to 70), which corresponds to loss of consciousness, does not increase the number of pharyngeal structures involved in collapse as compared with zolpidem-induced sleep endoscopy.15,17 We also hypothesized that DISE under recommended levels of propofol sedation does not increase upper airway collapsibility and dynamic compliance of pharyngeal structures. To test these hypotheses, individuals with OSA underwent zolpidem and propofol-induced sleep endoscopy.METHODSParticipantsThis pilot study was conducted at the Clinics Hospital, University of São Paulo, Brazil. Patients scheduled for pharyngeal surgery to treat OSA aged between 18 and 70 years were invited to participate. OSA was defined by an apnea-hypopnea index (AHI) of >5 events/h. Patients were excluded if they had nasal obstruction, significantly deviated nasal septum, nasal turbinate hypertrophy, or nasal polyps. Patients with uncontrolled heart failure, renal insufficiency, diabetes, or hyperthyroidism were also excluded. Patients were also excluded if taking medications that could affect upper airway muscle function, such as benzodiazepines and muscle relaxants.25 All participants gave written consent before study entry. The study was approved by the Clinics Hospital Ethics Committee and registered at clinicaltrials.gov (NCT03004014).ProtocolEach participant underwent a detailed clinical evaluation that included height, weight, and neck circumference measurements. All patients underwent a full polysomnography (PSG). During the following night, patients underwent zolpidem-induced sleep endoscopy. DISE with propofol was performed in the operating room, 2 days after zolpidem-induced sleep endoscopy.PSGPSG included electroencephalogram, electrooculogram, chin and tibial electromyography, electrocardiogram, oximetry, oronasal airflow (thermistor and pressure cannula), and measurements of rib cage and abdominal movements, snoring, and body position (Embla N7000; Natus, Inc., Middleton, WI). Apnea was defined as a reduction of ≥90% of the thermistor signal amplitude for ≥10 seconds. Hypopnea was defined as a reduction of ≥30% of nasal pressure amplitude for ≥10 seconds followed by oxygen desaturation ≥3% or arousal.26Instrumentation during both sleep endoscopiesAll participants were asked to sleep in a supine position with a comfortable pillow, with the head in a forward neutral position. Participants were fitted with a nasal mask, attached to a heated pneumotachometer (Hans-Rudolph, Kansas City, MO) and a differential pressure transducer (Validyne, Northridge, CA) for airflow measurement. Mask pressure was measured by another pressure transducer (Validyne, Northridge, CA). After nasal topical application of a decongestant (oxymetazoline 0.025%) and anesthetic (lidocaine 10%), a 1.9-mm-diameter pressure catheter (Millar, Houston, TX) and a 2.8-mm pediatric bronchoscope (BFXP-160F; Olympus, Tokyo, Japan) were inserted through the left and right nostrils, respectively. Both devices were passed through sealed ports of the nasal mask. The pharyngeal pressure catheter was placed at the level of the epiglottis. Initially, the bronchoscope’s tip was placed at the nasopharynx above the palate. Several sequences of flow-limited breaths, defined as a lack of increase in flow despite decreasing pharyngeal pressure,27 were recorded. If the patient presented repetitive obstructive apneas, low levels of continuous positive airway pressure (CPAP) was used to stabilize the airway and allow periods of stable flow limitation. After enough data were recorded at the velopharynx, the bronchoscope’s tip was moved forward to evaluate oropharyngeal and hypopharyngeal structures. All signals were captured at a sampling frequency of 200 Hz. Endoscopic images were sampled at 30 frames per second. BIS was used to assess the level of sedation during DISE (see below). During DISE, BIS and pulse oximetry monitors were recorded from an external camera. Physiologic signals, endoscopic image and the external camera image were synchronized and recorded on a personal computer using a data acquisition system (Power 1401; Cambridge Electronic Design, Cambridge, England). All sleep endoscopy procedures were performed by the same experienced medical team.Zolpidem-induced sleep endoscopySleep endoscopy during zolpidem-induced sleep was performed at the Sleep Laboratory during the night. All participants received zolpidem hemitartrate 10 mg orally 30 minutes prior to the start of the study. During zolpidem-induced sleep, participants were monitored using the same PSG montage, except for the nasal cannula and thermistor that were changed for a nasal mask and pneumotach as described above.Propofol-induced sleep endoscopyDISE was performed in the operating room during the day, just before the pharyngeal surgical procedure. Supplemental oxygen was not used before or during DISE with propofol. A target-controlled infusion system pump (Diprifusor; AstraZeneca) was used, starting with a target effect-site concentration of 1.5 μg/mL. The dose was increased by 0.1–0.2 μg/mL to achieve the recommended sedation depth: BIS level between 50 and 70 and Ramsay sedation scale level 5 (sluggish response to light glabellar tap or loud auditory stimulus).15,17 BIS levels were selected to be in accordance with BIS levels of sleep stages N2 and N3.28Data analysisThe pharyngeal structures involved in collapse were classified according to the VOTE Classification System29 during non-CPAP sleep. This classification considers the pharyngeal structure involved (velum, oropharynx, tongue base, and epiglottis) as well as the configuration of collapse (anteroposterior, lateral, or concentric) (Figure 1). Epiglottic collapse was considered both when the epiglottis was pushed by the tongue or if it collapsed independently. Partial airway collapse was not considered in the present study due to our previous experience with sleep endoscopy with simultaneous airflow recording suggesting that partial airway collapse does not influence airflow. Video image files from both sleep endoscopy studies were unidentified before being interpreted independently by 2 experienced investigators. A third investigator resolved any discrepancies. Only images from N2–N3 sleep during zolpidem-induced sleep and from BIS level of 50–70 and Ramsay sedation scale level 5 during DISE were included in the deidentified videos. The airway collapse patterns (VOTE endoscopic classification) were evaluated without CPAP use.Figure 1.: Representative examples taken during zolpidem- and propofol-induced sleep endoscopies showing agreement in the pattern of pharyngeal collapse.Patient A: Endoscopic view of concentric velum collapse; patient B: tongue base collapse; patient C: lateral pharyngeal wall collapse.Download FigurePeak inspiratory flow, NED, and minimum peripheral oxygen saturationIn order to compare upper airway collapsibility and functional pharyngeal size during zolpidem-induced sleep endoscopy and DISE with propofol, inspiratory peak flow and NED from flow-limited breaths were compared (Figure 2).30,31 Only breaths that were free of artifacts and arousals, taken from either atmospheric pressure or at the same CPAP level in each endoscopic procedure (zolpidem and propofol-induced sleep), were considered for analysis. Flow limitation was defined by the lack of increase in flow despite decreasing pharyngeal pressure.27 NED was calculated as follows: ((peak inspiratory flow – flow at minimum pharyngeal pressure)/peak inspiratory flow) × 100.31 Respiratory drive was estimated by the driving pressure (DP), calculated as: (pharyngeal pressure at end-expiration − minimum pharyngeal pressure). Since sedation could lead to a reduction in respiratory drive and upper airway narrowing/obstruction, a more pronounced desaturation during respiratory events could occur. Minimum peripheral oxygen saturation (SpO2) values during zolpidem- and propofol-induced sleep endoscopies were also compared.Figure 2.: Raw data recording of a sequence of flow-limited breaths in the same patient.A: peak inspiratory flow; B: flow at minimum pharyngeal pressure; C: pharyngeal pressure at end-expiration; D: minimum pharyngeal pressure. NED = ([A – B]/A) × 100. DP = C – D. DP = driving pressure; NED = negative effort dependence.Download FigureDuration of zolpidem- and propofol-induced sleep endoscopiesZolpidem-induced sleep endoscopy started when the lights were turned off with the patient positioned with instrumentation in place and ended when the endoscope was removed from the patient. DISE with propofol started at the beginning of the infusion of the sedative and ended when the endoscope was removed.Statistical analysisData for continuous variables are presented as means ± SDs or medians (first–third quartiles). Normality was assessed using the Kolmogorov-Smirnov test. A P value <.05 was considered significant. A paired t test or the nonparametric Wilcoxon signed-rank test was used to compare continuous variables (peak flow, NED, DP, minimum SpO2, duration of the sleep endoscopies, number of respiratory cycles analyzed, and pharyngeal pressure during NED assessment). McNemar’s test for paired proportions was used to test for changes between the number of pharyngeal structures involved in collapse. For each pharyngeal structure involved in collapse (velum, oropharynx, tongue, or epiglottis) 1 point was attributed. Changes in the VOTE classification between zolpidem- and propofol-induced sleep endoscopies were also tested using McNemar’s test. These statistical tests allow performing a comparison between data from zolpidem- and propofol-induced sleep in the same patient. Independent t test was used to compare the sleep apnea severity between the group without CPAP treatment and the group that needed CPAP treatment to induce airflow limitation. Effect size for the comparison of parametric data was described as the difference (95% confidence interval). For nonparametric data, effect size was calculated by dividing Z value (the number of SDs from the mean for a data point) by the square root of the number of tests performed.32 Statistical analyses were conducted using SPSS 18 (SPSS Inc., Chicago, IL) and Stata 11.0 (StataCorp, College Station, TX).RESULTSTwenty-one patients with OSA were studied and their characteristics are described in Table 1. The number of pharyngeal structures involved in collapse was similar during zolpidem-induced sleep and DISE with propofol (Table 2). Collapses of the velum, lateral pharyngeal wall, tongue, and epiglottis during zolpidem- and propofol-induced sleep are compared in Table 3 and Figure 3.Table 1. Participant characteristics.CharacteristicsValuesSex, % males67Age, years44 ± 9Neck circumference, cm42 ± 3BMI, kg/m231 ± 4Tonsil size, % Grade 153 Grade 233 Grade 314 Grade 40Mallampati classification, % I10 II33 III57 IV0Epworth Sleepiness Scale14 ± 7AHI, events/h44 ± 30AI, events/h20 ± 29HI, events/h24 ± 14Minimum SpO2,%75 ± 7Data are presented as means ± SDs unless otherwise indicated. AHI = apnea-hypopnea index; AI = apnea index; BMI = body mass index; HI = hypopnea index; SpO2 = peripheral oxygen saturation.Table 2. Number of upper airway structures with complete collapse.Zolpidem-Induced Sleep, n (%)Propofol-Induced Sleep, n (%)Difference (95% CI)P*Number of structures— 16 (28)3 (14) 212 (57)15 (71) 32 (9.5)1 (5) 41 (5.0)2 (9)Multilevel collapse15 (72)18 (86)14% (−12% to 40%).453CI = confidence interval. *McNemar’s test for paired proportions.Table 3. Site of pharyngeal collapse observed during zolpidem- and propofol-induced sleep endoscopies.Airway LevelZolpidem-Induced SleepPropofol-Induced SleepDifference (95% CI)PVelum, %.135* Anteroposterior14104 (−4 to 14) Concentric483810 (−9 to 28) Lateral3852−14 (−29 to 1)Oropharyngeal lateral walls, %57570 (−23 to 23)1.000Tongue base, %1419−5 (−14 to 4)1.000Epiglottis, %1933−14 (−29 to 1).250CI = confidence interval. *The 3 different configurations of vellum collapse were analyzed together.Figure 3.: Venn diagrams comparing the number of participants showing collapse at each upper airway structure and multilevel collapse during zolpidem- and propofol-induced sleep endoscopies.Download FigureThe mean duration of the zolpidem-induced sleep endoscopy was higher than during DISE with propofol (78.3 vs 30.8 minutes; P < .001). Mean propofol target concentration to reach the appropriate sedation level was 1.8 ± 0.3 μg/mL. Mean total dose of propofol was 322 ± 84 mg. The minimum SpO2 values during zolpidem-induced sleep and DISE with propofol were similar (75% and 78%, respectively; P = 0.09).Peak flow, NED, and DP analysis were performed in 17 participants (Table 4). Four participants were excluded from these analyses due to technical reasons. One participant was excluded because the pharyngeal pressure transducer failed. Three participants did not achieve stable flow limitation during comparable CPAP levels in both endoscopic studies. Five patients had stable flow limitation at atmospheric pressure, and no CPAP treatment was necessary. In 12 patients, CPAP treatment was necessary to induce stable flow limitation due to repetitive obstructive apneas. The group of patients who needed CPAP treatment had more severe sleep apnea (AHI: 54.8 vs 15.4 events/h; P = .002). The number of respiratory cycles analyzed was 987. On average, 33 ± 19 breaths were analyzed per patient during zolpidem-induced sleep endoscopy studies and 25 ± 14 breaths per patient during DISE with propofol. Propofol did not increase the peak inspiratory flow, NED, or the respiratory drive during sleep endoscopy (Table 4).Table 4. Peak flow, NED, and DP analysis.Zolpidem-Induced SleepPropofol-Induced SleepEffect Size or Difference (95% CI)PPeak flow, L/s0.326 (0.250–0.359)0.309 (0.265–0.358)0.05.758NED, %36.9 ± 20.542.9 ± 18−6.0 (−16 to 4).223DP, cm H2O17.1 (9.4–22.3)18.3 (9.6–22.6)0.03.831Breaths analyzed, n33 ± 2025 ± 148 (−1 to 16).078CPAP level, cm H2O3.4 ± 2.83.3 ± 2.70.1 (−0.1 to 0.3).154Data are presented as means ± SDs or medians (first–third quartile). Effect sizes were calculated for nonparametric data. Differences (95% CIs) were calculated for parametric data. CI = confidence interval; CPAP, continuous positive airway pressure; DP = driving pressure; NED = negative effort dependence.Nasal pressures during peak flow, NED, and DP analysis were 3.4 ± 2.8 cm H2O and 3.3 ± 2.7 cm H2O during zolpidem-induced sleep and DISE with propofol, respectively, reflecting low levels of CPAP used for these analyses.DISCUSSIONThe major findings of this pilot study are as follows: (1) propofol titrated to reach the strict recommended sedation levels did not increase the proportion of multilevel pharyngeal collapse as compared with zolpidem-induced sleep; (2) propofol did not increase pharyngeal collapsibility nor the compliance of the pharyngeal structures (estimated by peak inspiratory flow and NED) as compared with zolpidem-induced sleep; (3) propofol did not impair respiratory drive as compared with zolpidem-induced sleep.Sleep endoscopyDISE is a practical approach to detect the pharyngeal structures involved in pharyngeal collapse. Multilevel pharyngeal collapse may have implications for the surgical treatment of OSA.12 Vroegop et al22 observed multilevel collapse in 68% of patients with OSA who underwent DISE. In another study, Ravesloot and de Vries7 found multilevel collapse in 76% of the patients. The most common structure involved in collapse in both previous studies was the soft palate (81% and 83%), followed by the tongue base (47% and 56%).7,22 We observed multilevel collapse in 86% of patients during DISE with propofol. The most common structure involved in collapse in the present study was the soft palate (100%), followed by the lateral walls (57%). One possible explanation for the higher proportion of lateral wall involvement in our study is that we studied patients selected for lateral pharyngoplasty who frequently had prominent lateral wall muscles. A nonsignificant higher proportion of tongue and epiglottic collapse during propofol-induced sleep was observed. The findings of the present study confirm that multilevel collapse is common. Larger studies to address the influence of sedation on individual pharyngeal structures are warranted.Upper airway functionPeak inspiratory flow has been used to describe upper airway function and collapsibility. Marques et al33 used peak inspiratory flow during flow limitation to show improvement in upper airway patency at the lateral sleeping position as compared with the supine position in patients with OSA. Azarbarzin et al34 showed that peak inspiratory flow can estimate active critical closing pressure. NED is a marker of the dynamic compliance of the pharyngeal structure involved in collapse.24,35 In the present study, peak inspiratory flow and NED remained unchanged during zolpidem- and propofol-induced sleep, suggesting that upper airway patency and collapsibility were unaffected by propofol.SedationHillman et al17 observed loss of consciousness with propofol concentrations between 1.5 and 4 μg/mL. The average BIS values observed at loss of consciousness were between 50 and 70. A slight increase in genioglossus muscle tonus was observed at these propofol concentrations, but a sudden reduction in tonus at higher concentrations was reported.17 Eastwood et al18 and Hillman et al17 found good correlation between BIS levels and propofol effect site concentration: BIS significantly decreased with increasing the propofol effect site concentration. ‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬Rabelo et al16 compared OSA severity determined during natural sleep during the day and during propofol-induced sleep. The authors reported that propofol did not affect OSA severity but led to a lower minimum oxygen saturation as compared with natural sleep. However, a deeper sedation level may have been reached since a higher mean propofol target concentration was administered (2.3 ± 0.6 μg/mL). Using lower propofol doses (1.8 ± 0.3 μg/mL) that were able to achieve the recommended sedation depth, we observed similar minimum oxygen saturation as well as unaltered upper airway patency and collapsibility during zolpidem- and propofol-induced sleep in the present study. These results are in line with our previous observations that low doses of midazolam did not impair upper airway collapsibility determined by critical pharyngeal closing pressure (Pcrit), as compared with natural sleep.14Our study has several limitations. First, due to the instrumentation used in both studies, the sample size was small, especially to compare collapse at individual pharyngeal levels. The small sample size reduced the ability of this study to detect clinically important differences between zolpidem- and propofol-induced sleep endoscopies. However, this pilot study will be valuable to design a larger study, especially to detect the effect of sedation on the individual levels and configurations of pharyngeal collapse. Second, the pharyngeal catheter and endoscope used may have affected the site of collapse and airflow. A previous study has found that upper airway collapsibility was not altered by the presence of a catheter in the upper airway.36 Although there were 2 instruments in the airway, the endoscope was placed above the palate most of the time. Third, data acquired during zolpidem-induced sleep stages N2–N3 were compared with a BIS level between 50 and 70 during propofol-induced sleep because PSG was not feasible in the operating room. OSA is often more severe during rapid eye movement (REM) sleep. The exclusion of REM sleep from the analysis limits the conclusions of our findings to non-REM sleep only. Fourth, zolpidem could potentially have influenced sleep endoscopy outcomes. Upper airway collapsibility is not affected by zolpidem.37 However, zolpidem may increase upper airway responsiveness by unknown mechanisms. Although we cannot determine the exact influence of zolpidem in our findings, if present, it would have increased the differences between natural and propofol-induced sleep. Fifth, we have not assessed the reproducibility of pharyngeal collapse pattern classification. However, data from other studies confirmed good reproducibility and good interrater reliability of DISE.38–40 Last, the sample of patients with OSA studied were carefully selected for upper airway surgery and are not necessarily representative of the entire population with OSA.In this pilot study, propofol used to reach the recommended sedation levels did not significantly increase multilevel pharyngeal collapse or affect upper airway collapsibility and respiratory drive. Future studies with larger sample sizes should address the potential influence of sedation on upper airway function and individual levels of pharyngeal collapse.DISCLOSURE STATEMENTAll authors have seen and approved the manuscript. Work for this study was performed at the Universidade de São Paulo, São Paulo, Brazil. A.B.O. was supported by CNPQ; P.R.G. was supported by FAPESP and CNPQ. The authors report no conflicts of interest.ABBREVIATIONSAHIapnea-hypopnea indexBISbispectral indexCPAPcontinuous positive airway pressureDISEdrug-induced sleep endoscopyDPdriving pressureNEDnegative effort dependenceOSAobstructive sleep apneaPSGpolysomnographyREMrapid eye movementSpO2peripheral oxygen saturationREFERENCES1. Tufik S, Santos-Silva R, Taddei JA, Bittencourt LRA. Obstructive sleep apnea syndrome in the Sao Paulo Epidemiologic Sleep Study. Sleep Med. 2010;11(5):441–446. https://doi.org/10.1016/j.sleep.2009.10.005 CrossrefGoogle Scholar2. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328(17):1230–1235. https://doi.org/10.1056/NEJM199304293281704 CrossrefGoogle Scholar3. Sundaram S, Bridgman SA, Lim J, Lasserson TJ. Surgery for obstructive sleep apnoea. Cochrane Database Syst Rev. 200519):CD001004 Google Scholar4. Georgalas C, Garas G, Hadjihannas E, Oostra A. Assessment of obstruction level and selection of patients for obstructive sleep apnoea surgery: an evidence-based approach. J Laryngol Otol. 2010;124(1):1–9. https://doi.org/10.1017/S002221510999079X CrossrefGoogle Scholar5. Croft CB, Pringle M. Sleep nasendoscopy: a technique of assessment in snoring and obstructive sleep apnoea. Clin Otolaryngol Allied Sci. 1991;16(5):504–509. https://doi.org/10.1111/j.1365-2273.1991.tb01050.x CrossrefGoogle Scholar6. Hohenhorst W, Ravesloot MJL, Kezirian EJ, De Vries N. Drug-induced sleep endoscopy in adults with sleep-disordered breathing: technique and the VOTE classification system. Oper Tech Otolaryngol Head Neck Surg. 2012;23(1):11–18. https://doi.org/10.1016/j.otot.2011.06.001 CrossrefGoogle Scholar7. Ravesloot MJL, de Vries N. One hundred consecutive patients undergoing drug-induced sleep endoscopy: results and evaluation. Laryngoscope. 2011;121(12):2710–2716. https://doi.org/10.1002/lary.22369 CrossrefGoogle Scholar8. Van de Heyning PH, Badr MS, Baskin JZ, et al.. Implanted upper airway stimulation device for obstructive sleep apnea. Laryngoscope. 2012;122(7):1626–1633. https://doi.org/10.1002/lary.23301 CrossrefGoogle Scholar9. Salamanca F, Costantini F, Bianchi A, Amaina T, Colombo E, Zibordi F. Identification of obstructive sites and patterns in obstructive sleep apnoea syndrome by sleep endoscopy in 614 patients. Acta Otorhinolaryngol Ital. 2013;33261–266 Google Scholar10. Eichler C, Sommer JU, Stuck BA, Hörmann K, Maurer JT. Does drug-induced sleep endoscopy change the treatment concept of patients with snoring and obstructive sleep apnea?. Sleep Breath. 2013;17(1):63–68. https://doi.org/10.1007/s11325-012-0647-9 CrossrefGoogle Scholar11. Gillespie MB, Reddy RP, White DR, Discolo CM, Overdyk FJ, Nguyen SA. A trial of drug-induced sleep endoscopy in the surgical management of sleep-disordered breathing. Laryngoscope. 2013;123(1):277–282. https://doi.org/10.1002/lary.23506 CrossrefGoogle Scholar12. Fernández-Julián E, García-Pérez MÁ, García-Callejo J, Ferrer F, Martí F, Marco J. Surgical planning after sleep versus awake techniques in patients with obstructive sleep apnea. Laryngoscope. 2014;124(8):1970–1974. https://doi.org/10.1002/lary.24577 CrossrefGoogle Scholar13. Capasso R, Rosa T, Tsou DYA, et al.. Variable findings for drug-induced sleep endoscopy in obstructive sleep apnea with propofol versus dexmedetomidine. Otolaryngol Head Neck Surg. 2016;154(4):765–770. https://doi.org/10.1177/0194599815625972 CrossrefGoogle Scholar14. Genta PR, Eckert DJ, Gregorio MG, et al.. Critical closing pressure during midazolam-induced sleep. J Appl Physiol. 2011;111(5):1315–1322. https://doi.org/10.1152/japplphysiol.00508.2011 CrossrefGoogle Scholar15. De Vito A, Carrasco Llatas M, Vanni A, et al.. European position paper on drug-induced sedation endoscopy (DISE). Sleep Breath. 2014;18(3):453–465. https://doi.org/10.1007/s11325-014-0989-6 CrossrefGoogle Scholar16. Rabelo FA, Braga A, Küpper DS, et al.. Propofol-induced sleep: polysomnographic evaluation of patients with obstructive sleep apnea and controls. Otolaryngol Head Neck Surg. 2010;142(2):218–224. https://doi.org/10.1016/j.otohns.2009.11.002 CrossrefGoogle Scholar17. Hillman DR, Walsh JH, Maddison KJ, et al.. Evolution of changes in upper airway collapsibility during slow induction of anesthesia with propofol. Anesthesiology. 2009;111(1):63–71. https://doi.org/10.1097/ALN.0b013e3181a7ec68 CrossrefGoogle Scholar18. Eastwood PR, Platt PR, Shepherd K, Maddison K, Hillman DR. Collapsibility of the upper airway at different concentrations of propofol anesthesia. Anesthesiology. 2005;103(3):470–477. https://doi.org/10.1097/00000542-200509000-00007 CrossrefGoogle Scholar19. Kellner P, Herzog B, Plößl S, et al.. Depth-dependent changes of obstruction patterns under increasing sedation during drug-induced sedation endoscopy: results of a German monocentric clinical trial. Sleep Breath. 2016;20(3):1035–1043. https://doi.org/10.1007/s11325-016-1348-6 CrossrefGoogle Scholar20. Lo YL, Ni YL, Wang TY, et al.. Bispectral index in evaluating effects of sedation depth on drug-induced sleep endoscopy. J Clin Sleep Med. 2015;11(9):1011–1020. https://doi.org/10.5664/jcsm.5016 LinkGoogle Scholar21. Steinhart H, Kuhn-Lohmann J, Gewalt K, Constantinidis J, Mertzlufft F, Iro H. Upper airway collapsibility in habitual snorers and sleep apneics: evaluation with drug-induced sleep endoscopy. Acta Otolaryngol. 2000;120(8):990–994. https://doi.org/10.1080/00016480050218753 CrossrefGoogle Scholar22. Vroegop AV, Vanderveken OM, Boudewyns AN, et al.. Drug-induced sleep endoscopy in sleep-disordered breathing: report on 1,249 cases. Laryngoscope. 2014;124(3):797–802. https://doi.org/10.1002/lary.24479 CrossrefGoogle Scholar23. Isono S, Feroah TR, Hajduk EA, et al.. Interaction of cross-sectional area, driving pressure, and airflow of passive velopharynx. J Appl Physiol. 1997;83(3):851–859. https://doi.org/10.1152/jappl.1997.83.3.851 CrossrefGoogle Scholar24. Genta PR, Sands SA, Butler JP, et al.. Airflow shape is associated with the pharyngeal structure causing OSA. Chest. 2017;152(3):537–546. https://doi.org/10.1016/j.chest.2017.06.017 CrossrefGoogle Scholar25. Seda G, Tsai S, Lee-chiong T. Medication effects on sleep and breathing. Clin Chest Med. 2014;35(3):557–569. https://doi.org/10.1016/j.ccm.2014.06.011 CrossrefGoogle Scholar26. Berry RB, Brooks R, Gamaldo CE, et al.; for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. Version 2.2. Darien, IL: American Academy of Sleep Medicine; 2015 Google Scholar27. Genta PR, Edwards BA, Sands SA, et al.. Tube law of the pharyngeal airway in sleeping patients with obstructive sleep apnea. Sleep. 2016;39(2):337–343. https://doi.org/10.5665/sleep.5440 CrossrefGoogle Scholar28. Abdullah VJ, Lee DLY, Ha SCN, van Hasselt C. Sleep endoscopy with midazolam: sedation level evaluation with bispectral analysis. Otolaryngol Head Neck Surg. 2013;148(2):331–337. https://doi.org/10.1177/0194599812464865 CrossrefGoogle Scholar29. Kezirian EJ, Hohenhorst W, de Vries N. Drug-induced sleep endoscopy: the VOTE classification. Eur Arch Otorhinolaryngol. 2011;268(8):1233–1236. https://doi.org/10.1007/s00405-011-1633-8 CrossrefGoogle Scholar30. Isono S, Remmers JE, Tanaka A, Sho Y, Sato J, Nishino T. Anatomy of pharynx in patients with obstructive sleep apnea and in normal subjects. J Appl Physiol. 1997;82(4):1319–1326. https://doi.org/10.1152/jappl.1997.82.4.1319 CrossrefGoogle Scholar31. Genta PR, Owens RL, Edwards BA, et al.. Influence of pharyngeal muscle activity on inspiratory negative effort dependence in the human upper airway. Respir Physiol Neurobiol. 2014;20155–59. https://doi.org/10.1016/j.resp.2014.07.005 CrossrefGoogle Scholar32. Pallant JF. SPSS Survival Manual: A Step by Step Guide to Data Analysis. Philadelphia, PA: Open University Press; 2007 Google Scholar33. Marques M, Genta PR, Sands SA, et al.. Effect of sleeping position on upper airway patency in obstructive sleep apnea is determined by the pharyngeal structure causing collapse. Sleep. 2017;404–11 CrossrefGoogle Scholar34. Azarbarzin A, Sands SA, Taranto-Montemurro L, et al.. Estimation of pharyngeal collapsibility during sleep by peak inspiratory airflow. Sleep. 2017;40 CrossrefGoogle Scholar35. Marques M, Genta PR, Azarbarzin A, et al.. Retropalatal and retroglossal airway compliance in patients with obstructive sleep apnea. Respir Physiol Neurobiol. 2018;25898–103. https://doi.org/10.1016/j.resp.2018.06.008 CrossrefGoogle Scholar36. Maddison KJ, Shepherd KL, Baker VA, et al.. Effects on upper airway collapsibility of presence of a pharyngeal catheter. J Sleep Res. 2015;24(1):92–99. https://doi.org/10.1111/jsr.12193 CrossrefGoogle Scholar37. Carberry JC, Fisher LP, Grunstein RR, et al.. Role of common hypnotics on the phenotypic causes of obstructive sleep apnoea: paradoxical effects of zolpidem. Eur Respir J. 2017;50(6):1701344. https://doi.org/10.1183/13993003.01344-2017 CrossrefGoogle Scholar38. Kezirian EJ, White DP, Malhotra A, Ma W, McCulloch CE, Goldberg AN. Interrater reliability of drug-induced sleep endoscopy. Arch Otolaryngol Head Neck Surg. 2010;136(4):393–397. https://doi.org/10.1001/archoto.2010.26 CrossrefGoogle Scholar39. Carrasco-Llatas M, Zerpa-Zerpa V, Dalmau-Galofre J. Reliability of drug-induced sedation endoscopy: interobserver agreement. Sleep Breath. 2017;21(1):173–179. https://doi.org/10.1007/s11325-016-1426-9 CrossrefGoogle Scholar40. Rodriguez-Bruno K, Goldberg AN, McCulloch CE, Kezirian EJ. Test-retest reliability of drug-induced sleep endoscopy. Otolaryngol Head Neck Surg. 2009;140(5):646–651. https://doi.org/10.1016/j.otohns.2009.01.012 CrossrefGoogle Scholar Previous article Next article FiguresReferencesRelatedDetailsCited by Transverse Maxillary Deficiency Predicts Increased Upper Airway Collapsibility during Drug‐Induced Sleep EndoscopyThuler E, Seay E, Woo J, Lee J, Jafari N, Keenan B, Dedhia R and Schwartz A Otolaryngology–Head and Neck Surgery, 10.1002/ohn.258 The clinical application progress and potential of drug-induced sleep endoscopy in obstructive sleep apneaViana A, Estevão D and Zhao C Annals of Medicine, 10.1080/07853890.2022.2134586, Vol. 54, No. 1, (2908-2919), Online publication date: 31-Dec-2022. Natural sleep endoscopy in obstructive sleep apnea: A systematic reviewVan den Bossche K, Van de Perck E, Kazemeini E, Willemen M, Van de Heyning P, Verbraecken J, Op de Beeck S and Vanderveken O Sleep Medicine Reviews, 10.1016/j.smrv.2021.101534, Vol. 60, , (101534), Online publication date: 1-Dec-2021. Is There a Perfect Drug for Sedation in DISE?Matarredona-Quiles S, Pérez-Carbonell T, Ortega-Beltrá N, Vaz de Castro J, Alkan U and Carrasco-Llatas M Current Otorhinolaryngology Reports, 10.1007/s40136-021-00355-5 Volume 16 • Issue 5 • May 15, 2020ISSN (print): 1550-9389ISSN (online): 1550-9397Frequency: Monthly Metrics History Submitted for publicationJuly 8, 2019Submitted in final revised formJanuary 1, 2020Accepted for publicationJanuary 2, 2020Published onlineMay 15, 2020 Information© 2020 American Academy of Sleep MedicineKeywordsobstructive sleep apneapropofolendoscopyairway obstructionPDF download" @default.
• W3005264705 created "2020-02-14" @default.
• W3005264705 creator A5003002258 @default.
• W3005264705 creator A5024254786 @default.
• W3005264705 creator A5039814722 @default.
• W3005264705 creator A5044348863 @default.
• W3005264705 creator A5082070447 @default.
• W3005264705 creator A5091311035 @default.
• W3005264705 date "2020-05-15" @default.
• W3005264705 modified "2023-09-25" @default.
• W3005264705 title "Comparison of upper airway obstruction during zolpidem-induced sleep and propofol-induced sleep in patients with obstructive sleep apnea: a pilot study" @default.
• W3005264705 cites W1571826750 @default.
• W3005264705 cites W1972178287 @default.
• W3005264705 cites W1972994324 @default.
• W3005264705 cites W1974872033 @default.
• W3005264705 cites W1991763625 @default.
• W3005264705 cites W2020678594 @default.
• W3005264705 cites W2022584237 @default.
• W3005264705 cites W2025308968 @default.
• W3005264705 cites W2039127961 @default.
• W3005264705 cites W2068026499 @default.
• W3005264705 cites W2071780208 @default.
• W3005264705 cites W2076699461 @default.
• W3005264705 cites W2091128315 @default.
• W3005264705 cites W2097897338 @default.
• W3005264705 cites W2098742936 @default.
• W3005264705 cites W2107168729 @default.
• W3005264705 cites W2108534151 @default.
• W3005264705 cites W2111373781 @default.
• W3005264705 cites W2121234672 @default.
• W3005264705 cites W2124067200 @default.
• W3005264705 cites W2145077794 @default.
• W3005264705 cites W2145682509 @default.
• W3005264705 cites W2151867346 @default.
• W3005264705 cites W2162645075 @default.
• W3005264705 cites W2229991435 @default.
• W3005264705 cites W2292340024 @default.
• W3005264705 cites W2333343699 @default.
• W3005264705 cites W2342826542 @default.
• W3005264705 cites W2399916761 @default.
• W3005264705 cites W2405934760 @default.
• W3005264705 cites W2531747427 @default.
• W3005264705 cites W2546520404 @default.
• W3005264705 cites W2583888088 @default.
• W3005264705 cites W2638403458 @default.
• W3005264705 cites W2781196260 @default.
• W3005264705 cites W2808980570 @default.
• W3005264705 doi "https://doi.org/10.5664/jcsm.8334" @default.
• W3005264705 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7849792" @default.
• W3005264705 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32029070" @default.
• W3005264705 hasPublicationYear "2020" @default.
• W3005264705 type Work @default.
• W3005264705 sameAs 3005264705 @default.
• W3005264705 citedByCount "4" @default.
• W3005264705 countsByYear W30052647052021 @default.
• W3005264705 countsByYear W30052647052022 @default.
• W3005264705 countsByYear W30052647052023 @default.
• W3005264705 crossrefType "journal-article" @default.
• W3005264705 hasAuthorship W3005264705A5003002258 @default.
• W3005264705 hasAuthorship W3005264705A5024254786 @default.
• W3005264705 hasAuthorship W3005264705A5039814722 @default.
• W3005264705 hasAuthorship W3005264705A5044348863 @default.
• W3005264705 hasAuthorship W3005264705A5082070447 @default.
• W3005264705 hasAuthorship W3005264705A5091311035 @default.
• W3005264705 hasBestOaLocation W30052647051 @default.
• W3005264705 hasConcept C105922876 @default.
• W3005264705 hasConcept C111919701 @default.
• W3005264705 hasConcept C118552586 @default.
• W3005264705 hasConcept C2775841894 @default.
• W3005264705 hasConcept C2776006263 @default.
• W3005264705 hasConcept C2776277131 @default.
• W3005264705 hasConcept C2777123777 @default.
• W3005264705 hasConcept C2777935920 @default.
• W3005264705 hasConcept C2778205975 @default.
• W3005264705 hasConcept C2778333281 @default.
• W3005264705 hasConcept C2781210498 @default.
• W3005264705 hasConcept C2781326671 @default.
• W3005264705 hasConcept C41008148 @default.
• W3005264705 hasConcept C42219234 @default.
• W3005264705 hasConcept C548259974 @default.
• W3005264705 hasConcept C71924100 @default.
• W3005264705 hasConceptScore W3005264705C105922876 @default.
• W3005264705 hasConceptScore W3005264705C111919701 @default.
• W3005264705 hasConceptScore W3005264705C118552586 @default.
• W3005264705 hasConceptScore W3005264705C2775841894 @default.
• W3005264705 hasConceptScore W3005264705C2776006263 @default.
• W3005264705 hasConceptScore W3005264705C2776277131 @default.
• W3005264705 hasConceptScore W3005264705C2777123777 @default.
• W3005264705 hasConceptScore W3005264705C2777935920 @default.
• W3005264705 hasConceptScore W3005264705C2778205975 @default.
• W3005264705 hasConceptScore W3005264705C2778333281 @default.
• W3005264705 hasConceptScore W3005264705C2781210498 @default.
• W3005264705 hasConceptScore W3005264705C2781326671 @default.
• W3005264705 hasConceptScore W3005264705C41008148 @default.
• W3005264705 hasConceptScore W3005264705C42219234 @default.
• W3005264705 hasConceptScore W3005264705C548259974 @default.
• W3005264705 hasConceptScore W3005264705C71924100 @default.
• W3005264705 hasIssue "5" @default.

• next